Phytoglycoprotein isolated from Dioscorea batatas Decne promotes intestinal epithelial wound healing.
10.1016/S1875-5364(20)60014-0
- Author:
Ji-Yun KIM
1
;
Young-Min LEE
1
;
Jong-Pil PARK
2
;
Kye-Taek LIM
3
;
Sei-Jung LEE
4
Author Information
1. Department of Pharmaceutical Engineering, Daegu Haany University, Gyeongsan 38610, Republic of Korea.
2. Department of Food Science and Technology, Chung-Ang University, Anseong 17546, Republic of Korea.
3. Division of Animal Science, Chonnam National University, Gwangju, 61186, Republic of Korea.
4. Department of Pharmaceutical Engineering, Daegu Haany University, Gyeongsan 38610, Republic of Korea. Electronic address: sjlee@dhu.ac.kr.
- Publication Type:Journal Article
- Keywords:
Cell migration;
Dioscorea batatas Decne (DBD) glycoprotein;
F-actin;
Intestinal epithelial cells;
Mouse colitis;
p38 MAPK
- From:
Chinese Journal of Natural Medicines (English Ed.)
2020;18(10):738-748
- CountryChina
- Language:English
-
Abstract:
Dioscorea batatas Decne (DBD) has been used to heal various illnesses of the kidney and intestine as an herbal medicine in Asia. As a source of therapeutic agents, many glycoproteins have been isolated from mushrooms and plants, but the functional role of glycoprotein in intestinal epithelial wound healing has not been understood yet. In the present study, we investigated the wound healing potentials of the 30 kDa glycoprotein (DBD glycoprotein) isolated from DBD in human intestinal epithelial (INT-407) cells. We found that DBD glycoprotein (100 μg·mL) significantly increased the motility of INT-407 cells for 24 h by activating protein kinase C (PKC). DBD glycoprotein stimulated the activation of p38 mitogen-activated protein kinase (MAPK), which is responsible for the phosphorylation of NF-κB inhibitor α (IκBα). DBD glycoprotein increased the level of profilin-1 (PFN1), α-actinin and F-actin expression via activation of transcription factor, nuclear factor-kappa B (NF-κB) during its promotion of cell migration. Experimental mouse colitis was induced by adding dextran sulfate sodium (DSS) to the drinking water at a concentration of 4% (W/V) for 7 days. We figured out that administration of DBD glycoprotein (10 and 20 mg·kg) lowers the levels of disease activity index and histological inflammation in DSS-treated ICR mice. In this regard, we suggest that DBD glycoprotein has ability to promote the F-actin-related migration signaling events via activation of PKC and NF-κB in intestinal epithelial cells and prevent inflammatory bowel disease.
